To test the hypothesis that distention of the main pulmonary artery (MPA) due to partial ballon inflation causes a reflex production of pulmonary arterial hypertension and hyperpnea with regulation arterial PCO2, the following studies are proposed: (1) Patterns of hemodynamic, respiratory, blood gas and acid-base balance responses to acute and chronic pulmonary artery balloon distention (PABD) will be determined in the conscious dog. Dogs will be prepared by implantation of a triple lumen balloon catheter in the MPA. The MPA will be distended to produce a significant elevation in pulmonary artery pressure distal to the balloon without a change in right ventricular, end-diastolic pressure, aortic pressure and cardiac output. Right ventricular, pulmonary artery and aortic pressures; minute ventilation; tidal volume; and tidal PCO2 and PO2; and breathing frequency will be measured continuously before, during and after PABD. Arterial blood gas and acid-base status, physiological dead space and cardiac outputs will be determined before and during PABD. (2) To eliminate hypoxia as a cause of the PABD responses, dogs will breathe 100 percent 02. (3) To determine the extent to which PABD responses are a CO2 coupled phenomenon, dogs will be anesthesized and the respiratory rate and tidal volume will be controlled. (4) The reversibility of chronic PABD induced PA hypertension wll be determined by intermittent inflation and deflation of the balloon for a period of 4-8 weeks. (5) Possible reflex pathways and receptors involved in these responses will be investigated by pharmacological and surgical interventions of known nervous pathways and surgical isolation of the MPA. (6) The nature and extent of changes in the pulmonary vasculature will be studied under light and electron microscopy.